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Fractional Diffusion Modulates Distribution of Action Potential Duration in Fibrotic Atrial Strands

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Ugarte J.P.
Tobon C.
Palacio L.C.
Andrade-Caicedo H.
Saiz J.

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TY - GEN T1 - Fractional Diffusion Modulates Distribution of Action Potential Duration in Fibrotic Atrial Strands AU - Ugarte J.P. AU - Tobon C. AU - Palacio L.C. AU - Andrade-Caicedo H. AU - Saiz J. UR - http://hdl.handle.net/11407/5721 PB - IEEE Computer Society AB - Background: Fibroblast proliferation, as a component of the fibrotic process, plays a role in structural remodeling, but also can alter the electrophysiology of the cardiomyocytes. Aim: To study the action potential duration dispersion (dAPD) in fibrotic atrial strands, where fibroblasts exerts both, structural and electrical influence on the propagation, using a fractional diffusion model. Methods: The Courtemanche model of human atrial cell is implemented under chronic atrial fibrillation (AF) remodeling conditions. The atrial strands are designed as 1D domains, having a fibrotic portion localized in the middle. Fibrosis is modeled taking into account an electrical component, implemented by coupling a number of fibroblasts to a single cardiomyocyte, and a structural component, implemented through a q-order fractional derivative. Results: The variations of q define two dAPD dispersion regimes. For q < 1.4, the fibrosis density and the number of fibroblast per cardiomyocyte do not alter the dAPD. For q ? 1.4, the dAPD depends on the fibrosis spatial characteristics. Conclusion: This study shows that the structural component of fibrosis, modeled using fractional diffusion, modulates the spatial dAPD in a domain including electrical coupling of cardiomyocytes and fibroblasts, under chronic AF conditions. © 2018 Creative Commons Attribution. ER - @misc{11407_5721, author = {Ugarte J.P. and Tobon C. and Palacio L.C. and Andrade-Caicedo H. and Saiz J.}, title = {Fractional Diffusion Modulates Distribution of Action Potential Duration in Fibrotic Atrial Strands}, year = {}, abstract = {Background: Fibroblast proliferation, as a component of the fibrotic process, plays a role in structural remodeling, but also can alter the electrophysiology of the cardiomyocytes. Aim: To study the action potential duration dispersion (dAPD) in fibrotic atrial strands, where fibroblasts exerts both, structural and electrical influence on the propagation, using a fractional diffusion model. Methods: The Courtemanche model of human atrial cell is implemented under chronic atrial fibrillation (AF) remodeling conditions. The atrial strands are designed as 1D domains, having a fibrotic portion localized in the middle. Fibrosis is modeled taking into account an electrical component, implemented by coupling a number of fibroblasts to a single cardiomyocyte, and a structural component, implemented through a q-order fractional derivative. Results: The variations of q define two dAPD dispersion regimes. For q < 1.4, the fibrosis density and the number of fibroblast per cardiomyocyte do not alter the dAPD. For q ? 1.4, the dAPD depends on the fibrosis spatial characteristics. Conclusion: This study shows that the structural component of fibrosis, modeled using fractional diffusion, modulates the spatial dAPD in a domain including electrical coupling of cardiomyocytes and fibroblasts, under chronic AF conditions. © 2018 Creative Commons Attribution.}, url = {http://hdl.handle.net/11407/5721} }RT Generic T1 Fractional Diffusion Modulates Distribution of Action Potential Duration in Fibrotic Atrial Strands A1 Ugarte J.P. A1 Tobon C. A1 Palacio L.C. A1 Andrade-Caicedo H. A1 Saiz J. LK http://hdl.handle.net/11407/5721 PB IEEE Computer Society AB Background: Fibroblast proliferation, as a component of the fibrotic process, plays a role in structural remodeling, but also can alter the electrophysiology of the cardiomyocytes. Aim: To study the action potential duration dispersion (dAPD) in fibrotic atrial strands, where fibroblasts exerts both, structural and electrical influence on the propagation, using a fractional diffusion model. Methods: The Courtemanche model of human atrial cell is implemented under chronic atrial fibrillation (AF) remodeling conditions. The atrial strands are designed as 1D domains, having a fibrotic portion localized in the middle. Fibrosis is modeled taking into account an electrical component, implemented by coupling a number of fibroblasts to a single cardiomyocyte, and a structural component, implemented through a q-order fractional derivative. Results: The variations of q define two dAPD dispersion regimes. For q < 1.4, the fibrosis density and the number of fibroblast per cardiomyocyte do not alter the dAPD. For q ? 1.4, the dAPD depends on the fibrosis spatial characteristics. Conclusion: This study shows that the structural component of fibrosis, modeled using fractional diffusion, modulates the spatial dAPD in a domain including electrical coupling of cardiomyocytes and fibroblasts, under chronic AF conditions. © 2018 Creative Commons Attribution. OL Spanish (121)
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Abstract
Background: Fibroblast proliferation, as a component of the fibrotic process, plays a role in structural remodeling, but also can alter the electrophysiology of the cardiomyocytes. Aim: To study the action potential duration dispersion (dAPD) in fibrotic atrial strands, where fibroblasts exerts both, structural and electrical influence on the propagation, using a fractional diffusion model. Methods: The Courtemanche model of human atrial cell is implemented under chronic atrial fibrillation (AF) remodeling conditions. The atrial strands are designed as 1D domains, having a fibrotic portion localized in the middle. Fibrosis is modeled taking into account an electrical component, implemented by coupling a number of fibroblasts to a single cardiomyocyte, and a structural component, implemented through a q-order fractional derivative. Results: The variations of q define two dAPD dispersion regimes. For q < 1.4, the fibrosis density and the number of fibroblast per cardiomyocyte do not alter the dAPD. For q ? 1.4, the dAPD depends on the fibrosis spatial characteristics. Conclusion: This study shows that the structural component of fibrosis, modeled using fractional diffusion, modulates the spatial dAPD in a domain including electrical coupling of cardiomyocytes and fibroblasts, under chronic AF conditions. © 2018 Creative Commons Attribution.
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